Aim:Mild traumatic brain injury (TBI) may cause cognitive and emotional behavioural disorders. Following head trauma, magnesium concentration in brain tissues decreases; consequently, low magnesium concentrations are responsible for secondary injury processes. We recently demonstrated that magnesium acetyl taurate can effectively pass from systemic circulation into brain tissue, but its functional effectiveness in head trauma is yet unclear. The aim of this study was to investigate the effects of different magnesium forms on tissue damage and behavioural impairment after mild TBI. Material and Methods:Rats were divided into 5 groups (control, trauma, magnesium sulphate, magnesium citrate, magnesium acetyl taurate) and following head trauma, empathy-like behaviour, anxiety-like behaviour (elevated plus maze and open field tests), and depression (forced swim test) were measured. The rats were then sacrificed 12 days later. Oxytocin, vasopressin and receptors levels in the amygdala and prefrontal cortex regions were measured. Histopathological damage (with haematoxylin-eosin staining) and apoptosis (with caspase-3 immunohistochemistry) was evaluated. Results:Following head trauma, anxiety-like behaviour and depression tests did not change; empathy-like behaviour deteriorated on the 3rd day and improved gradually on the 6th and 12th days. Oxytocin, vasopressin and vasopressin v1b receptor levels decreased in the amygdala; morphological damage and apoptosis were significant. Magnesium acetyl taurate effectively ameliorated histopathological deteriorations and improved vasopressin and v1b receptor levels in the amygdala. Transient deterioration of empathy-like behaviour was impeded only in magnesium taurate treatment. Conclusion:Magnesium acetyl taurate can be a promising agent candidate to prevent structural and functional damage in traumatic brain injury.